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During simulated mechanical ventilation in pediatric and adult models, bias flow and nebulizer type and position impact aerosol drug delivery.
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Current guidelines support using in combination more than one class of long-acting bronchodilator for COPD patients whose symptoms are not controlled by mono-therapy. This 2-week, multi-center (34 sites), randomized, modified-blind, parallel group study evaluated the efficacy and safety of concomitant treatment with nebulized arformoterol (the formoterol(R,R)-isomer) BID and tiotropium DPI QD.
For patients with respiratory allergy due to birch pollen and mild persistent asthma, sublingual immunotherapy added to low-dose inhaled corticosteroids appears effective in maintaining long-term seasonal asthma control, representing a safe opportunity to reduce the cumulative amount of delivered corticosteroids.
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Urban emergency department.
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This is a single center, retrospective chart review study at a major children's hospital in an urban location. To qualify for this study, participants must have been admitted to the PICU with a diagnosis of status asthmaticus. There were a total of 188 participants between the ages of two and nineteen, excluding patients receiving antibiotics for pneumonia. PASS was calculated upon PICU admission. Subjects were put into one of three categories based on PASS: ≤ 7 (mild), 8-11 (moderate), and ≥ 12 (severe). The groups were compared based on different variables, including length of continuous albuterol and PICU stay.
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clinicaltrials.gov: NCT01323634; NCT01323621; NCT01706328. GlaxoSmithKline study codes: HZC113109; HZC112352; RLV116974.
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The urinary excretion of leukotriene E4 (LTE4) was measured in subjects presenting for emergency treatment of airway obstruction. A total of 72 subjects presenting with airway obstruction performed peak flow determinations before and after three treatments with nebulized albuterol given at 20-min intervals. Of these subjects, 22 more than doubled their peak flow rates, while 19 failed to increase their peak flow rates more than 25% during the treatment period. These groups were designated "responders" and "nonresponders," respectively. Urinary LTE4 excretion was determined in 16 of the 22 responders and 12 of the 19 nonresponders as well as 13 normal subjects by precolumn extraction, analytic reversed-phase high-performance liquid chromatography, and enzyme immunoassay. In the normal subjects the urinary LTE4 excretion was significantly (p less than 0.0001) less than the urinary LTE4 measured in the responder subjects, but not less than the urinary LTE4 excretion in the nonresponder group (p = 0.071). The enhanced recovery of LTE4 from the urine of subjects with acutely reversible airway narrowing is consistent with a bronchoconstrictor role for the cysteinyl leukotrienes in spontaneous acute asthma.
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Twenty-six asthmatic patients who were hospitalised following an acute asthmatic attack and who had a peak expiratory flow of less than 50% predicted, without hypercapnia, received 5 mg. of salbutamol delivered by a micronebulizer LSA on admission (HO). At H1, 10 mg of additional salbutamol were nebulised in cases where there had been an increase of less than 20% of the PEF. At H2, all the subjects received steroid therapy. Group 1 in which success was defined by an increase of 20% of peak flow judged at H1 and H2, and group II where the increase in peak flow was less than 20%. Group II benefited at H2 by treatment with theophylline or salbutamol intravenously given in a randomised fashion. At H8 the 2 treatments were associated in group II in cases of failures. 15 men, and 11 women aged 40 +/- 17 suffering from severe asthma (65% of Charpin Stage IV) were included. The mean peak flow at HO was 32 +/- 9% of the predicted PEF. 21 subjects, or 81% improved their peak flow by more than 20% at H2. The toleration for salbutamol was very good from the cardiovascular point of view. At HO there was no clinical criteria nor peak flow assessment which would enable one to predict the failures from nebulized salbutamol for a given subject. Nevertheless a level of dyspnoea of greater than 5 on Borg's scale and a peak flow of less than 150 l/min made failure likely.(ABSTRACT TRUNCATED AT 250 WORDS)
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The results of this open-label, randomised study showed that SFC provided greater asthma control than CC in the management of persistent asthma.
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Three severity items had poor validity, i.e., cyanosis, depressed cerebral function, and I:E ratio (p > 0.05). Three items had poor inter-rater reliability, i.e., breath sound quality, air entry, and I:E ratio. These items were omitted and three new clinical scores were constructed from the remaining items. Clinical scoring system comprised retractions, dyspnea, O2 saturation, respiratory rate and wheezing (rangeof score 0-10) gave the best accuracy and inter-rater variability and were chosen for clinical use-Siriraj Clinical Asthma Score (SCAS).
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At the conclusion of this article, the readers should be able to 1) describe the laryngeal findings in patients who use combination therapy for asthma, 2) discuss the mechanism of laryngeal irritation from the use of inhalers, and 3) describe possible mechanisms for reducing laryngeal irritation and secondary dysphonia from the use of inhalers.
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Lung slices (150 μm) were prepared from male Balb/C mice. Changes in intrapulmonary airway lumen area were recorded and analysed by phase-contrast microscopy. Relaxation to PGE(2) and salbutamol were assessed following various levels of pre-contraction with methacholine, serotonin or endothelin-1, as well as following overnight incubation with PGE(2) or salbutamol. The mechanism of PGE(2)-mediated relaxation was explored using selective EP antagonists (EP(1/2) AH6809; EP(4) L-161982) and Ca(2+)-permeabilized slices, where airway responses are due to regulation of Ca(2+)-sensitivity alone.
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From 1993 to 2004, bronchiolitis accounted for approximately 198 outpatient visits representing 8.75 million visits for children younger than 2 years. Among this same age group, the overall rate was 103 (95% CI, 83, 124) per 1000 US children and 17 (95% CI, 13, 20) per 1000 visits. When we compared bronchiolitis visits to all nonbronchiolitis visits, we found that those with bronchiolitis were less likely to be from the Northeast (12% vs 22%; P < .05) and more likely to be admitted to the hospital (2% vs 0.4%; P < .05). Fifty-two percent were prescribed albuterol; diagnostic tests were uncommon.
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1. The accumulation of cyclic AMP stimulated by salmeterol, a long-acting beta 2-adrenoceptor agonist and by isoprenaline, a non-selective beta-adrenoceptor agonist have been compared in the B50 neuroblastoma cell line. 2. Salmeterol produced a concentration-dependent increase in the accumulation of total [3H]-cyclic AMP in B50 cells yielding an EC50 value of 37 nM which was lower than that obtained with isoprenaline (294 nM). The maximum response to salmeterol was only 46% of that obtained with isoprenaline. 3. The beta 2-adrenoceptor antagonist, ICI 118551, inhibited the responses to both salmeterol (apparent KD 2.2 nM) and isoprenaline (apparent KD 1.6 nM). However, the beta 1-adrenoceptor antagonist, atenolol, produced no significant effect at concentrations up to 100 microM. 4. Salmeterol (1 microM) changed the concentration-response curve of isoprenaline in the manner of a partial agonist interacting with a full agonist. The KD of salmeterol obtained from the interaction was 55.6 nM. 5. Whereas salmeterol has a slow onset of action in airway smooth muscle compared to other beta 2-adrenoceptor agonists, in B50 monolayers both salmeterol and isoprenaline produced a rapid increase in cyclic AMP accumulation (t1/2 1.1 min and 0.4 min respectively). 6. Despite the existence of cyclic AMP efflux mechanisms that exist in this cell line it was possible to investigate the duration of agonist action by measuring intracellular levels of the second messenger. Replacement of drug-containing medium with fresh buffer led to a rapid reduction in intracellular levels of cyclic AMP in isoprenaline-stimulated cells whereas cyclic AMP accumulation was sustained for much longer periods in salmeterol-stimulated cells. However, the persistent action of salmeterol could be reversed by the addition of a beta2-selective antagonist.7. These results confirm that salmeterol has a high affinity, but low efficacy (relative to isoprenaline) for beta2-adrenoceptors coupled to cyclic AMP accumulation and that the drug persists at its site of action for long periods in the B50 neuronal cell line.
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Chronic obstructive pulmonary disease (COPD) is a common disease characterized by airflow obstruction and lung hyperinflation leading to dyspnea and exercise capacity limitation.
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Isothermal titration microcalorimetry was the principal technique used to measure the adsorption behaviour of surfactants to salbutamol sulphate. A Malvern particle size analyzer was also employed to provide size data on the interactions between the surfactant and powder suspensions.
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This is the first comparison of two combination therapies, fluticasone propionate/salmeterol and ipratropium bromide/albuterol (salbutamol), for the treatment of patients with COPD.
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Placebo-controlled trials have established the benefits of both long-acting beta-agonist and inhaled corticosteroid therapy for COPD patients as individual therapies. This review, which included trials allowing comparisons between LABA and ICS, has shown that the two therapies confer similar benefits across the majority of outcomes, including the frequency of exacerbations and mortality. Use of long-acting beta-agonists appears to confer a small additional benefit in terms of improvements in lung function compared to inhaled corticosteroids. On the other hand, inhaled corticosteroid therapy shows a small advantage over long-acting beta-agonist therapy in terms of health-related quality of life, but inhaled corticosteroids also increase the risk of pneumonia. This review supports current guidelines advocating long-acting beta-agonists as frontline therapy for COPD, with regular inhaled corticosteroid therapy as an adjunct in patients experiencing frequent exacerbations.
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This study was a retrospective chart review of all of the patients with a primary diagnosis of severe, non-life-threatening COPD exacerbations admitted from January 2007 to June 2008 at a university-affiliated hospital. Each patient's inhaled bronchodilator treatment regimen, including potential for nebulization to metered-dose inhaler (MDI) with valved holding chamber (VHC) conversion, was assessed.
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The mean flow rates for the compressors evaluated without a nebulizer attached ranged from 6.6 L/minute (LifeCare Freedom-neb; LifeCare International, Lafayette, CO) to 12.2 L/minute (DeVilbiss Pulmo-Aide; DeVilbiss Health Care, Somerset, PA). Flow rates for the nebulizer/compressor combinations ranged from 2.08 L/minute (Pari LC Jet Proneb; Pari Respiratory Equipment, Richmond, VA) to 5.42 L/minute (Puritan Bennett Raindrop; Puritan Bennett, Lenexa, KS/Omron Compare; Omron, Health Care,Vernon Hills, IL). Using the repeated measure ANOVA model, the interaction between flow rate and device was significant (P < 0.001) for both percentage of particles in the respirable range and log volume median diameter. It was observed that the percentage of particles in the respirable range for the Pari LC Jet did not increase across flow rates in contrast to the other 4 nebulizers. All comparisons to the Pari LC Jet at 2 L/minute were significant.
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The established place of regular long-acting beta2-adrenoceptor agonists at step 3 in asthma management guidelines has evolved as a consequence of evidence showing additive effects of salmeterol and formoterol on exacerbation rates, resulting in a putative inhaled corticosteroid sparing effect. There is however, evidence to show that although long-acting beta2-adrenoceptor agonists facilitate using a lower dose of inhaled corticosteroid, this may occur at the expense of suboptimal anti-inflammatory control. This is likely to be the case especially with fixed dose combination inhalers where it is not possible to properly titrate anti-inflammatory therapy with inhaled corticosteroids without also inadvertently overtreating with unnecessarily high doses of long-acting beta2-adrenoceptor agonists. Most patients with mild to moderate persistent asthma can be adequately controlled on monotherapy with inhaled corticosteroid in low or medium dosage, which is considerably cheaper than concomitant use of a long-acting beta2-adrenoceptor agonist. Subsensitivity to long-acting beta2-adrenoceptor agonists is a predictable pharmacological phenomenon which occurs despite concomitant inhaled corticosteroid therapy and occurs more readily for bronchoprotective than bronchodilator effects. Subsensitivity of salbutamol protection against bronchoconstrictor stimuli occurs in patients receiving concomitant long-acting beta2-adrenoceptor agonists, which may be due to beta2-adrenoceptor down-regulation or prolonged receptor occupancy. Prospective large scale long-term studies are required to further define the clinical relevance of beta2-adrenoceptor polymorphisms, to look at clinical control outcomes as well as propensity for subsensitivity. It would therefore make more sense to first of all optimize the dose of anti-inflammatory therapy with inhaled corticosteroid and to then consider adding a long-acting beta2-adrenoceptor agonist for patients who are poorly controlled.
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Randomized, double-blind, double-dummy parallel group, placebo-controlled, multicenter trial of asthmatics requiring inhaled beta-adrenergic bronchodilators for symptom control.
Seventy-five patients were assessed. Overall, 11 (31%) of 36 in the prednisone group required hospitalization compared with 19 (49%) of 39 in the placebo group (P = .10). Among the sickest patients (initial pulmonary index > 10), 7 (32%) of 22 prednisone-treated patients required hospitalization compared with 13 (72%) of 18 placebo-treated patients (P < .05). Among patients who had a suboptimal response to initial beta 2-agonist therapy and who therefore would have been hospitalized had treatment been restricted to 2 hours, 9 (45%) of 20 in the prednisone group ultimately required hospitalization when duration of care was extended 2 additional hours compared with 15 (83%) of 18 in the placebo group (P < .05). In addition, prednisone-treated patients had a significantly greater improvement in median pulmonary index (5.0 vs 3.0, P < .001).
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Indacaterol is a once-daily, long-acting β(2)-agonist bronchodilator that improves dyspnoea and health status in patients with moderate-to-severe COPD. While its bronchodilator effects have been shown to be maintained in different patient subgroups, effects on clinical outcomes in certain subgroups are not yet defined.
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The gene expression of ion channels and aquaporin was increased in mild ARDSp, but not ARDSexp. In ARDSp, intravenous salbutamol resulted in higher gene expression of alveolar epithelial sodium channel (0.20 ± 0.07 vs. 0.68 ± 0.24, p < 0.001), aquaporin-1 (0.44 ± 0.09 vs. 0.96 ± 0.12, p < 0.001) aquaporin-3 (0.31 ± 0.12 vs. 0.93 ± 0.20, p < 0.001), and Na-K-ATPase-α (0.39 ± 0.08 vs. 0.92 ± 0.12, p < 0.001), whereas intratracheal salbutamol increased the gene expression of aquaporin-1 (0.46 ± 0.11 vs. 0.92 ± 0.06, p < 0.001) and Na-K-ATPase-α (0.32 ± 0.07 vs. 0.58 ± 0.15, p < 0.001). In ARDSexp, the gene expression of ion channels and aquaporin was not influenced by salbutamol. Morphological and functional variables and edema formation were not affected by salbutamol in any of the ARDS groups, regardless of the route of administration.
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An increase in serious adverse events with both regular formoterol and regular salmeterol in chronic asthma has been demonstrated in comparison with placebo in previous Cochrane reviews. This increase was significant in trials that did not randomise participants to an inhaled corticosteroid, but less certain in the smaller numbers of participants in trials that included an inhaled corticosteroid in the randomised treatment regimen.
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Patients with persistent asthma well controlled by low doses of triamcinolone cannot be switched to salmeterol monotherapy without risk of clinically significant loss of asthma control.